製品番号: HY-113465

Leukotriene E4

Name: Leukotriene E4
Brand: MedChemExpress
SKU: HY-113465
Price: 430.00 USD
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(別名: LTE4; ロイコトリエンE4)

1 Cited Publications

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Based on 1 publication(s) in Google Scholar

Leukotriene E4 (LTE4) is a stable final metabolite of cysteinyl leukotrienes, produced by immune cells such as mast cells and eosinophils. Leukotriene E4 serves as a key biomarker for evaluating asthma severity, Aspirin (HY-14654) sensitivity, and mast cell activation disorders. Leukotriene E4 is a full functional agonist of CysLT₁R, which induces sustained intracellular calcium mobilization and Erk phosphorylation. Leukotriene E4 mediates inflammation in a P2Y₁₂ receptor-dependent manner. Leukotriene E4 can be used in the research of asthma and non-steroidal anti-inflammatory drug-exacerbated respiratory diseases.
The product specifications provided below refer solely to the active content of Leukotriene E4.

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研究用途以外に使用した場合、当社は一切の責任を負いかねます。

純度 : 99.61%
CAS 番号: 75715-89-8
分子式: C₂₃H₃₇NO₅S
分子量:439.61

保管条件:

Solution, -20°C, 2 years

Leukotriene E4 構造式

CAS 番号: 75715-89-8

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生物活性
- 製品説明
- IC₅₀ & Target
- Cellular Effect
- 体外実験
- 体内実験
化学情報
Publications (1)
純度とドキュメンテーション
参考文献
Calculators
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関連分類
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生物活性

製品説明

Leukotriene E4 (LTE4) is a stable final metabolite of cysteinyl leukotrienes, produced by immune cells such as mast cells and eosinophils. Leukotriene E4 serves as a key biomarker for evaluating asthma severity, Aspirin (HY-14654) sensitivity, and mast cell activation disorders. Leukotriene E4 is a full functional agonist of CysLT₁R, which induces sustained intracellular calcium mobilization and Erk phosphorylation. Leukotriene E4 mediates inflammation in a P2Y₁₂ receptor-dependent manner. Leukotriene E4 can be used in the research of asthma and non-steroidal anti-inflammatory drug-exacerbated respiratory diseases^[1]^[2]^[3].
The product specifications provided below refer solely to the active content of Leukotriene E4.

IC₅₀ & Target

^[1]^[2]

Human Endogenous Metabolite

CysLT₁

P2Y14 Receptor

Endogenous Metabolite アイソフォーム固有の製品をすべて表示 :

Leukotriene Receptor アイソフォーム固有の製品をすべて表示 :

Calcium Channel アイソフォーム固有の製品をすべて表示 :

ERK アイソフォーム固有の製品をすべて表示 :

P2Y Receptor アイソフォーム固有の製品をすべて表示 :

Cellular Effect

Cell Line	Type	Value	Description	References
Sf9	IC₅₀	9.83 μM Compound: Leukotrien E4	TP_TRANSPORTER: inhibition of E217betaG uptake (E217betaG: 0.055 uM) in membrane vesicles from Mrp2-expressing Sf9 cells TP_TRANSPORTER: inhibition of E217betaG uptake (E217betaG: 0.055 uM) in membrane vesicles from Mrp2-expressing Sf9 cells	[PMID: 11306690]

体外実験

Lipid Inflammatory MediatorsCytokines & Chemokines

Lipid Inflammatory Mediators

Leukotriene E4 induces concentration-dependent sustained intracellular calcium mobilization in LAD2 human mast cells, with an EC₅₀ of 1.67 nM^[1].
Leukotriene E4 induces only a very weak, non-sustained intracellular calcium mobilization response in LUVA human mast cells, with no detectable EC₅₀^[1].
Leukotriene E4 induces concentration-dependent intracellular calcium mobilization in HEK293T cells transfected with CYSLTR1, with an EC₅₀ of 83.2 nM^[1].
Leukotriene E4 (100 nM; 2-60 min) induces sustained phosphorylation of Erk in LAD2 human mast cells, and the activation signal remains detectable after 60 minutes^[1].
Leukotriene E4 (100 nM; 2-60 min) induces transient phosphorylation of Erk in LUVA human mast cells, with no sustained activation observed within 60 minutes^[1].
Leukotriene E4 (1-100 nM; 15 min) induces PTX-sensitive, MK571-resistant ERK phosphorylation in Chinese hamster ovary cells stably expressing human P2Y₁₂ receptors, with activation initiating at 1 nM and reaching a plateau at 100 nM^[2].
Leukotriene E4 (500 nM) induces calcium influx in LAD2 human mast cells, and this response is not inhibited by the P2Y₁₂ antagonist 2-MesAMP (HY-125989)^[2].
Leukotriene E4 (100 nM) induces the production of PGD₂ in the human mast cell line LAD2, and the generation of this product is completely dependent on the P2Y₁₂ receptor^[2].
Leukotriene E4 (1 μM; 10 min) does not induce the expression of CD62P (an activation marker) in human blood platelets^[2].

Lipid Inflammatory Mediators

Cytokines & Chemokines

Leukotriene E4 (100 nM; 2-6 h) induces the expression of CCL4 and CSF2 mRNA and protein in LAD2 human mast cells via a CysLT1-dependent mechanism, with potency equivalent to or stronger than that of LTD4^[1].
Leukotriene E4 (100 nM; 2-6 h) induces only extremely weak CCL4 mRNA and protein expression in LUVA human mast cells, with much lower potency relative to LTD4^[1].
The induction of CCL4 mRNA expression in human mast cell line LAD2 by Leukotriene E4 (100 nM; 2 h) depends on the MEK/Erk pathway and intracellular/extracellular Ca²⁺, but is independent of Gi/o proteins or the PPAR-γ signaling pathway^[1].
Leukotriene E4 (100 nM; 5 min-2 h) requires prolonged exposure (2 h) to induce full CCL4 mRNA expression in LAD2 human mast cells, whereas short-term exposure (5 min) only elicits weak activity^[1].
Leukotriene E4 (100-500 nM; 6 h) induces high levels of MIP-1β production in LAD2 human mast cells, and this production process is mainly dependent on the P2Y₁₂ receptor; the P2Y₁₂ antagonist 2-MesAMP inhibits more than 50% of its production, while P2Y₁₂ shRNA knockdown almost completely blocks this production process^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Real Time qPCR^[1]

Cell Line:

LAD2 human mast cells
Concentration:

100 nM
Incubation Time:

2 h (mRNA analysis); 6 h (protein analysis)
Result:

Consistently induced CCL4 and CSF2 mRNA and protein expression, matching or exceeding the potency of LTD4.
Induced mRNA expression was fully inhibited by pre-treatment with 100 nM Montelukast (HY-13315A) for 10 minutes.
Induced mRNA expression was not affected by 1 μM HAMI3379 (HY-112248A).

Real Time qPCR^[1]

Cell Line:

LUVA human mast cells
Concentration:

100 nM
Incubation Time:

2 h (mRNA analysis); 6 h (protein analysis)
Result:

Induced only very weak CCL4 mRNA and protein expression.
Showed negligible activity compared to LTD4.

Western Blot Analysis^[1]

Cell Line:

LAD2 human mast cells
Concentration:

100 nM
Incubation Time:

2, 5, 7, 10, 15, 30, 60 minutes
Result:

Induced Erk phosphorylation that peaked later than LTD4-induced phosphorylation.
Induced Erk phosphorylation remained detectable for 60 minutes, showing sustained activation compared to the gradual decrease observed with LTD4.

Western Blot Analysis^[1]

Cell Line:

LUVA human mast cells
Concentration:

100 nM
Incubation Time:

2, 5, 7, 10, 15, 30, 60 minutes
Result:

Induced Erk phosphorylation that peaked at a similar time to LTD4-induced phosphorylation.
Induced Erk phosphorylation was shorter in duration than the sustained activation observed in LAD2 cells.

Real Time qPCR^[1]

Cell Line:

LAD2 human mast cells
Concentration:

100 nM
Incubation Time:

2 h
Result:

Induced CCL4 mRNA expression was potently inhibited by U0126, BAPTA-AM, and EDTA.
Induced CCL4 mRNA expression was not modified by pertussis toxin, GW9662, or T0070907.

Real Time qPCR^[1]

Cell Line:

LAD2 human mast cells
Concentration:

100 nM
Incubation Time:

5 minutes, 2 hours
Result:

2-hour exposure induced CCL4 mRNA expression levels similar to those induced by LTD4.
5-minute exposure induced significantly lower CCL4 mRNA expression than 5-minute exposure to LTD4.

Real Time qPCR^[1]

Cell Line:

CYSLTR1-knockdown LAD2 human mast cells
Concentration:

100 nM
Incubation Time:

2 h (mRNA analysis); 6 h (protein analysis)
Result:

Induced CCL4 mRNA and protein expression was almost completely abrogated compared to empty vector control LAD2 cells.

Western Blot Analysis^[2]

Cell Line:

Chinese hamster ovary (CHO) cells stably transfected with human P2Y₁₂ receptor (forward orientation) or empty reverse construct control
Concentration:

500 nM (stimulation); 1 nM, 100 nM (dose-response analysis)
Incubation Time:

15 min (stimulation)
Result:

Exhibited robust ERK phosphorylation in response to LTE₄, with activation detectable at doses as low as 1 nM and reaching a plateau at 100 nM.
Showed partial block of LTE₄-induced ERK activation by pretreatment with 2-MesAMP.
Showed LTE₄-induced ERK activation sensitive to PTX and resistant to MK571.
Showed no ERK phosphorylation in response to LTE₄ (reverse orientation P2Y₁₂ construct cells).

ELISA Assay^[2]

Cell Line:

LAD2 human mast cells
Concentration:

100 nM, 500 nM
Incubation Time:

6 h
Result:

Induced substantial MIP-1β production at 100 nM and 500 nM, exceeding levels induced by LTD₄ and IgE plus anti-IgE.
Blocked LTE₄-mediated MIP-1β production by >50% after pretreatment with 2-MesAMP.
Nearly abrogated LTE₄-induced MIP-1β production after P2Y₁₂ receptor knockdown (reducing mRNA expression by ~90%).
Slightly (non-significantly) decreased the response to LTE₄ after CysLT₁R knockdown.

体内実験

Lipid Inflammatory MediatorsCytokines & ChemokinesInnate Immunity

Lipid Inflammatory Mediators

Cytokines & Chemokines

Innate Immunity

Leukotriene E4 (2.2 nmol; intranasal administration; once daily for 3 consecutive days) significantly enhances allergen-induced pulmonary eosinophilia, bronchovascular inflammation, and goblet cell metaplasia in sensitized BALB/c mice^[2].

Lipid Inflammatory Mediators

Innate Immunity

Leukotriene E4 (2.2 nmol; intranasal administration; once daily for 3 consecutive days) enhances allergen-induced pulmonary inflammation in wild-type C57BL/6 mice, but this activity is significantly attenuated in mice lacking the P2Y₁₂ receptor^[2].
Leukotriene E4 (2.2 nmol; intranasal administration; once daily for 3 consecutive days) enhances allergen-induced pulmonary inflammation in BALB/c mice, and this effect is independent of the classical CysLT₁R and CysLT₂R receptors^[2].
The enhanced allergen-induced pulmonary inflammation effect in sensitized BALB/c mice mediated by Leukotriene E4 (2.2 nmol; intranasal administration; once daily for 3 consecutive days) is completely dependent on platelets^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

BALB/c (male, 6-8 wk old, OVA (HY-W250978)-sensitized asthma model)^[2]
Dosage:

2.2 nmol
Administration:

i.n.; once daily; 3 days (30 minutes before each OVA challenge)
Result:

Significantly enhanced bronchoalveolar lavage fluid eosinophilia.
Increased bronchovascular inflammation score per 15 bronchi to levels approaching those of mice challenged with 1% OVA.
Increased PAS-positive goblet cells per mm of bronchial basal lamina to levels approaching those of mice challenged with 1% OVA.
Modestly increased lung expression of IL-13 and MUC5AC mRNA.

Animal Model:

C57BL/6 wild-type (male and female, 6-8 wk old, OVA-sensitized asthma model); C57BL/6 p2ry12^-/^- (age- and sex-matched, OVA-sensitized asthma model)^[2]
Dosage:

2.2 nmol
Administration:

i.n.; once daily; 3 days (30 minutes before each OVA challenge)
Result:

Potentiated bronchoalveolar lavage fluid eosinophilia, goblet cell metaplasia, and bronchovascular infiltration in wild-type mice.
Severely blunted all LTE4-mediated potentiation of these inflammatory endpoints in P2Y₁₂ receptor-deficient mice.

Animal Model:

BALB/c wild-type (6-8 wk old, OVA-sensitized asthma model); BALB/c Cysltr1/Cysltr2^-/^- (OVA-sensitized asthma model)^[2]
Dosage:

2.2 nmol
Administration:

i.n.; once daily; 3 days (30 minutes before each OVA challenge)
Result:

Potentiated OVA-induced bronchoalveolar lavage fluid eosinophilia, goblet cell metaplasia, and bronchovascular inflammation completely intact in CysLT₁R and CysLT₂R double-deficient mice, matching responses in wild-type controls.

Animal Model:

BALB/c (male, 6-8 wk old, platelet-depleted, OVA-sensitized asthma model)^[2]
Dosage:

2.2 nmol
Administration:

i.n.; once daily; 3 days (30 minutes before each OVA challenge)
Result:

Completely eliminated LTE4-mediated potentiation of airway eosinophilia, bronchovascular inflammation, and goblet cell metaplasia, with effects identical to P2Y₁₂ receptor blockade via clopidogrel.

Related Protocols :

化学情報

CAS 番号 75715-89-8
性状 Liquid
分子量 439.61
分子式 C₂₃H₃₇NO₅S
Color Colorless to light yellow
SMILES

CCCCC/C=C\C/C=C\C=C\C=C\[C@@H](SC[C@H](N)C(O)=O)[C@@H](O)CCCC(O)=O
別名

LTE4; ロイコトリエンE4
Structure Classification
- Ketones, Aldehydes, Acids
Initial Source
- Endogenous metabolite
輸送条件

Room temperature in continental US; may vary elsewhere.
保管条件

Solution, -20°C, 2 years

Publications (1)

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Nat Commun

Molecular insights into ligand recognition and signaling of OXGR1. [Abstract]

2025 Dec 18;16(1):11205. PMID: 41413034

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バッチを選択:

純度: 99.98%

Assay: 99.98%

ee.: 99.98%

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COA (2659 KB)
元素分析報告書 (2659 KB)
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参考文献

[1]. Foster HR, et al. Leukotriene E4 is a full functional agonist for human cysteinyl leukotriene type 1 receptor-dependent gene expression. Scientific reports. 2016 Feb 02;6:20461.

[2]. Paruchuri, S., et al. (2009). Leukotriene E4–induced pulmonary inflammation is mediated by the P2Y12 receptor. Journal of Experimental Medicine, 206(11), 2543-2555.

[3]. Marquette M, et al. Urinary Leukotriene E4 as a Biomarker in NSAID-Exacerbated Respiratory Disease (N-ERD): a Systematic Review and Meta-analysis. Current allergy and asthma reports. 2022 Dec;22(12):209-229.

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Leukotriene E4

1 Cited Publications

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Leukotriene E4

MedChemExpress（MCE）の使用を引用している文献 Leukotriene E4

Endogenous Metabolite アイソフォーム固有の製品をすべて表示

Leukotriene Receptor アイソフォーム固有の製品をすべて表示

Calcium Channel アイソフォーム固有の製品をすべて表示

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P2Y Receptor アイソフォーム固有の製品をすべて表示

生物活性

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IC₅₀ & Target

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Publications (1)

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最近チェックした製品

Leukotriene E4

MedChemExpress（MCE）の使用を引用している文献 Leukotriene E4

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Leukotriene Receptor アイソフォーム固有の製品をすべて表示

Calcium Channel アイソフォーム固有の製品をすべて表示

ERK アイソフォーム固有の製品をすべて表示

P2Y Receptor アイソフォーム固有の製品をすべて表示

生物活性

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体内実験

化学情報

Publications (1)

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Leukotriene E4 関連分類

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